Rat IL-4 ELISA kit
- Known as:
- Rat Interleukin-4 Enzyme-linked immunosorbent assay test reagent
- Catalog number:
- BEK1105
- Product Quantity:
- 96 T
- Category:
- Elisa Kits
- Supplier:
- Biospect
- Gene target:
- Rat IL-4 ELISA kit
Related genes to: Rat IL-4 ELISA kit
- Gene:
- IL4 NIH gene
- Name:
- interleukin 4
- Previous symbol:
- -
- Synonyms:
- BSF1, IL-4, BCGF1, BCGF-1, MGC79402
- Chromosome:
- 5q31.1
- Locus Type:
- gene with protein product
- Date approved:
- 1988-08-10
- Date modifiied:
- 2016-10-05
- Gene:
- TLR2 NIH gene
- Name:
- toll like receptor 2
- Previous symbol:
- -
- Synonyms:
- TIL4, CD282
- Chromosome:
- 4q31.3
- Locus Type:
- gene with protein product
- Date approved:
- 1998-06-25
- Date modifiied:
- 2016-10-25
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- In response to the Letter by Song and Luan, we clarify the route and rationale of interleukin-4 (IL-4) administration in our published study. Recombinant mouse IL-4 was administered intracerebroventricularly as a mechanistic intervention to engage central IL-4/STAT6 signaling, whereas the reference to systemic administration in Section 4.4 was intended to describe systemic CGRP receptor blockade. We further clarify the intracerebroventricular procedure, including guide cannula implantation, anesthesia, recovery, and subsequent IL-4 administration. We also acknowledge that the non-IL-4 groups did not undergo matched guide-cannula implantation or intracerebroventricular vehicle administration, which represents a limitation when interpreting the in vivo effects specifically associated with IL-4. These clarifications define the appropriate scope of interpretation of the in vivo IL-4 findings. - Source: PubMed
Publication date: 2026/09/20
Li ZichaoGe Zhaoming - Osteoarthritis (OA) is a leading cause of global disability, with no available therapies that effectively halt disease progression. Impairment of macrophage efferocytosis, the clearance of apoptotic cells, is implicated in OA pathogenesis, yet the underlying mechanisms remain poorly understood. This study investigates the role of the anti‑inflammatory cytokine interleukin‑4 (IL‑4) in regulating macrophage efferocytosis during OA. - Source: PubMed
Publication date: 2026/09/19
Zhang HaipingYu ZiliangGao DagongXia FeiLi YixuanHe JiafengLiu WeiZhou Xiaozhong - Airway remodeling represents a key pathological feature of severe asthma. Although the interleukin-13 (IL-13) R130Q variant is associated with increased disease severity, its specific contribution to airway remodeling remains unclear. - Source: PubMed
Publication date: 2026/08/25
He YafangSun JingyiLi LuanluanBai ShashaZhai XiaojiaTian YePan QinBao YixiaoDing Guodong - Air pollution-associated allergic airway inflammation is an increasing public health concern. Interleukin‑4 (IL‑4) and interleukin‑13 (IL‑13), which activate the Signal Transducer and Activator of Transcription 6 (STAT6) pathway, a central mediator of allergic airway inflammation, may modulate the respiratory toxicities of pollutants. The present study describes the generation and validation of a stable STAT6 luciferase reporter assay in human airway epithelial cells for evaluating environmental toxicants that modulate STAT6 signaling. Human bronchial epithelial 16HBE14o cells were transduced with a STAT6-responsive luciferase reporter using a lentiviral vector, followed by optimization of puromycin selection and multiplicity of infection, and monoclonal isolation by limiting dilution. A stable clone with strong and reproducible induction across serial passages was selected. Reporter responsiveness was validated by IL-4/IL-13 stimulation, and STAT6 dependence was confirmed using selective STAT6, STAT5, and STAT3 inhibitors. Assay performance was quantified by Z'-factor analysis, which indicated reproducible signal separation. Furthermore, the assay was applied to individual air-pollution constituents, and benzo[b]fluoranthene and particulate matter significantly increased STAT6 reporter activity. This method provides a scalable approach for measuring STAT6 activity in airway epithelial cells and for prioritizing environmental toxicants that modulate allergic airway signaling. - Source: PubMed
Publication date: 2026/08/25
Moonwiriyakit AekkachaPothipan PhattarinToyingsirikul DhanpisitSantiwong PawitLusawat Sirapop - IFNγ and IL-4, the canonical Th1 and Th2 cytokines, typically induce opposing macrophage polarization. Beyond their frequent coexistence and mutual antagonism in pathological settings, a synergistic crosstalk may also exist and remains to be defined. Through integrated transcriptomic, epigenomic, and CRISPR-based analyses, we identify that co-exposure to IL-4 and IFNγ results in an intermediate macrophage polarization state in murine macrophages, associated with a cohort of synergistically activated genes. We show that this synergistic activation is mediated by co-binding of STAT6 and STAT1 at regulatory regions marked with pronounced H3K27Ac accumulation and is dependent on the BRD4 cofactor. Deletion of either STAT factor or disruption of their binding motifs abolishes the synergistic transcriptional response. Our data support a model in which chromatin openness induced by one cytokine facilitates binding of the opposing cytokine-activated STAT transcription factor (TF), contributing to synergistic gene activation. We further show that IRF1, an IFNγ-induced TF whose expression persists in the presence of IL-4, is indispensable for a substantial subset of this program. Importantly, single-cell RNA sequencing of the PyMT murine breast cancer model reveals an in vivo tumor-associated macrophage subset showing STAT1 and STAT6 activation and is enriched for the synergistic gene signature. - Source: PubMed
Varga ZsófiaPoscher AnnaVáradi Eszter AnnaCinege GyöngyiIzsán AntalErdős EdinaBenyhe-Kis BernadettTihanyi Anna ZsuzsannaTzerpos PetrosBene KrisztiánHalász LászlóGémes NikolettNeuperger PatríciaTóth MártaMigh EdePóliska SzilárdSzebeni Gábor JWalter Jolán EDániel BenceCsörgő BálintNagy LászlóCzimmerer Zsolt